NM  Vol.2 No.3 , September 2011
Mitogen-Activated Protein Kinase Pathways Following Traumatic Brain Injury
ABSTRACT
The mechanisms underlying the secondary or delayed cell death in the hippocampus and cerebral hemisphere after traumatic brain injury (TBI) have been poorly understood. Recent data suggesting that TBI may have relationship with both an inflammatory and a neurodegenerative factors are also presented. Mitogen-activated protein kinases (MAPK), which play a crucial role in signal transduction, are activated by phosphorylation in response to a variety of mitogenic signals. In this article, we review the clinical and experimental evidence for brain damage after TBI. In addition, the MAPK pathways, closely involved in signal transduction after TBI, which could therefore be a new and potentially effective therapeutic target in TBI. Further investigations are therefore necessary to better understand cerebral traumatic damage and delineate the best practice strategies needed to improve the patient outcomes after TBI.

Cite this paper
nullN. Otani, H. Nawashiro, K. Nagatani, S. Takeuchi, H. Kobayashi and K. Shima, "Mitogen-Activated Protein Kinase Pathways Following Traumatic Brain Injury," Neuroscience and Medicine, Vol. 2 No. 3, 2011, pp. 208-216. doi: 10.4236/nm.2011.23028.
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